ArticleLaboratory investigation; a journal of technical methods and pathology2015
Basal cells of the human airways acquire mesenchymal traits in idiopathic pulmonary fibrosis and in culture.
Article in Laboratory investigation; a journal of technical methods and pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 62 citations in OpenAlex.
- Desmoplakin loss in alveolar epithelium drives Wnt/β-Catenin-mediated extracellular matrix remodeling and fibrotic signaling in vitro.Molecular biology reports · 2026Article
- Effects of LATS1/2 kinases inhibition on lung epithelial cells in a regeneration model.Molecular and cellular biochemistry · 2026Article
- Cilostazol mitigates amiodarone-induced pulmonary toxicity and fibrosis by regulating the cAMP/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition in rats.Scientific reports · 2026Article
- Control of airway basal stem cell-mediated lung repair by TGF-β signaling.Science advances · 2026Article
- How the Fibrotic Lung Microenvironment Regulates Stem Cell Behavior: Immune Cues, Extracellular Matrix Remodeling, and Therapeutic Implications.Analytical cellular pathology (Amsterdam) · 2026Review
- Inflammation and epithelial-mesenchymal transition in a CFTR-depleted human bronchial epithelial cell line revealed by proteomics and human organ-on-a-chip.The FEBS journal · 2025Article
- The Non-Antibacterial Effects of Azithromycin and Other Macrolides on the Bronchial Epithelial Barrier and Cellular Differentiation.International journal of molecular sciences · 2025Article
- Magneto-acoustic protein nanostructures for non-invasive imaging of tissue mechanics in vivo.Nature materials · 2024Article
- Bronchial Progenitor Cells in Obstructive and Neoplastic Lung Disease: A Pilot Study.Journal of clinical medicine · 2024Article
- Intercellular Communication in Airway Epithelial Cell Regeneration: Potential Roles of Connexins and Pannexins.International journal of molecular sciences · 2023Review
- Precise identification of cell states altered in disease using healthy single-cell references.Nature genetics · 2023Article
- Lung extracellular matrix modulates KRT5Nature communications · 2023Article
- Article
- Basal Cell-derived WNT7A Promotes Fibrogenesis at the Fibrotic Niche in Idiopathic Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2023Article
- Proteomic Fingerprint of Lung Fibrosis Progression and Response to Therapy in Bleomycin-Induced Mouse Model.International journal of molecular sciences · 2023Article
- Article
- Central lung gene expression associates with myofibroblast features in idiopathic pulmonary fibrosis.BMJ open respiratory research · 2023Article
- Pulmonary endogenous progenitor stem cell subpopulation: Physiology, pathogenesis, and progress.Journal of intensive medicine · 2023Review
- Airway basal cells show a dedifferentiated KRT17Nature communications · 2022Article
- Bronchial epithelium epithelial-mesenchymal plasticity forms aberrant basaloid-like cells in vitro.American journal of physiology. Lung cellular and molecular physiology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with high morbidity and mortality. The cellular source of the fibrotic process is currently under debate with one suggested mechanism being epithelial-to-mesenchymal transition (EMT) in the alveolar region. In this study, we show that airway epithelium overlying fibroblastic foci in IPF contains a layer of p63-positive basal cells while lacking ciliated and goblet cells. This basal epithelium shows increased expression of CK14, Vimentin and N-cadherin while retaining E-cadherin. The underlying fibroblastic foci shows both E- and N-cadherin-positive cells. To determine if p63-positive basal cells were able to undergo EMT in culture, we treated VA10, a p63-positive basal cell line, with the serum replacement UltroserG. A sub-population of treated cells acquired a mesenchymal phenotype, including an E- to N-cadherin switch. After isolation, these cells portrayed a phenotype presenting major hallmarks of EMT (loss of epithelial markers, gain of mesenchymal markers, increased migration and anchorage-independent growth). This phenotypic switch was prevented in p63 knockdown (KD) cells. In conclusion, we show that airway epithelium overlying fibroblastic foci in IPF lacks its characteristic functional identity, shows increased reactivity of basal cells and acquisition of a partial EMT phenotype. This study suggests that some p63-positive basal cells are prone to phenotypic changes and could act as EMT progenitors in IPF.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.